Immunoregulation in Chronic Infectious Disease: Schistosomiasis as a Model

This review summarizes the current evidence that both the induction and amelioration of disease in hepatosplenic schistosomiasis are immunologically mediated. We hypothesize that the extent of disease depends on the balance between activation of immunologic disease processes and immunologic suppression of disease processes. In mice the major disease-producing process is granuloma formation, a cell-mediated hypersensitivity reaction to parasite egg antigens. There appear to be multiple possible pathways for the natural suppression of this hypersensitivity. Recent work on murine schistosomiasis in our own and other laboratories has detected 3 immunoregulatory systems and has developed tools to explore each of them. 1. Results from serum transfer experiments suggest that antibody-mediated immunologic blockade plays a role in modulating granuloma formation. Accurate radioimmunoassays, developed for the quantification of antibody to the major granuloma-producing antigens, may be useful in the elucidation of the mechanism of blockade. 2. Cell transfer experiments have demonstrated that suppressor T cells can inhibit the cell-mediated immune hypersensitivity reaction to schistosome eggs. Lymphokine assays, measuring specific suppressor cells may enable us to monitor this activity in man. 3. Mitogen-induced lymphocyte DNA synthesis is suppressed in chronic schistosomiasis. With this system we can examine nonspecific schistosome-induced suppressor cells from persons with schistosomiasis